scholarly journals Regulation of UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosamine-1-phosphate transferase by retinoic acid in P19 cells

1999 ◽  
Vol 338 (2) ◽  
pp. 561-568 ◽  
Author(s):  
Joachim D. MEISSNER ◽  
Andreas NAUMANN ◽  
Walter H. MUELLER ◽  
Renate J. SCHEIBE
Keyword(s):  
Enzyme Activity ◽  
Retinoic Acid ◽  
Hormonal Regulation ◽  
Fold Increase ◽  
Enzymic Activity ◽  
P19 Cells ◽  
All Trans Retinoic Acid ◽  
Teratocarcinoma Cells ◽  
Regulatory Impact ◽  
Dolichol Pathway

UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosamine-1-phosphate transferase (GPT) is the first enzyme in the dolichol pathway of protein N-glycosylation, and is implicated in the developmental programmes of a variety of eukaryotes. In the present study we describe the effects of all-trans-retinoic acid (RA) on the levels of GPT protein and enzymic activity, and on the transcription rate of the GPT gene, in mouse P19 teratocarcinoma cells. RA caused a dose-dependent and protein-synthesis-dependent induction of enzyme activity. The maximum induction of GPT activity (about 3-fold) required 2 days of exposure to 1 µM RA. Induced GPT activity also resulted in an increase in the rate of incorporation of [3H]mannose into Glc3Man9GlcNAc2. Enzymic activities paralleled GPT gene expression. The GPT gene was induced (2-fold) after 7 h of RA treatment. An approx. 3-fold increase in a 48 kDa GPT protein and approx. 4-fold increases in the levels of three GPT transcripts (1.8, 2.0 and 2.2 kb) were observed after 2 days of RA treatment. The enhanced levels of GPT protein and mRNAs began to decline 3 days after the initiation of differentiation, and GPT expression was down-regulated during cellular differentiation. GPT activity decreased about 2.8-fold to a constant level in differentiated P19 cells. The results indicate that the RA-induced enzyme activity was mainly determined by increased transcription of the GPT gene. RA-treated P19 cells were about 4-fold more resistant to tunicamycin, a fungal antibiotic which inhibits GPT, than were control cells. In addition, GPT activity in membranes from RA-treated P19 cells exhibited approx. 4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity. Furthermore, increased GPT activity had regulatory significance with regard to the rate of incorporation of [3H]mannose into Glc3Man9GlcNAc2-P-P-dolichol and into glycoproteins. Together, the data provide additional insights into the hormonal regulation of GPT and present evidence that the RA-mediated induction of GPT has a regulatory impact on the dolichol pathway.

scholarly journals Expression of Sec61alpha in F9 and P19 teratocarcinoma cells after retinoic acid treatment

2003 ◽  
Vol 63 (2) ◽  
pp. 245-252 ◽  
Author(s):  
L. R. Ferreira ◽  
C. E. E. Velano ◽  
E. C. Braga ◽  
C. C. Paula ◽  
H. Martélli-Junior ◽  
...  
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Acid Treatment ◽  
Secretory Proteins ◽  
P19 Cells ◽  
Retinoic Acid Treatment ◽  
Teratocarcinoma Cell ◽  
F9 Cells ◽  
Teratocarcinoma Cells ◽  
Differentiation Stage

Nascent procollagen peptides and other secretory proteins are transported across the endoplasmic reticulum (RE) membrane through a protein-conducting channel called the translocon. Sec61alpha, a multispanning membrane translocon protein, has been implicated as essential for translocation of polypeptides chains into the cisterns of the ER. However, it is not known whether Sec61alpha is ubiquitously expressed in collagen producing teratocarcinoma cells. Furthermore, the production, expression, and utilization of Sec61alpha may depend on the cell differentiation stage. Stem cells from many cultured teratocarcinoma cell lines such as F9 and P19 cells are capable of differentiation in response to low retinoic acid concentrations. This differentiation of the tumorigenic stem cells results in tumorigenicity loss. For this study, mouse F9 and P19 teratocarcinoma cells were grown in culture medium treated with or without retinoic acid. Expression of Sec61alpha was determined by reverse trancriptase polimerase chain reaction (RT-PCR). In untreated conditions, F9 cells expressed undetected Sec61alpha amounts. It was also demonstrated that Sec61alpha expression is stimulated in F9 cells after retinoic acid treatment for 72 hours. No changes were found in Sec61alpha expression in P19 cells after retinoic acid treatment. These data indicate that the expression of Sec61alpha is enhanced with retinoic acid induced differentiation of F9 teratocarcinoma cells.

scholarly journals Retinoic acid induces liver/bone/kidney-type alkaline phosphatase gene expression in F9 teratocarcinoma cells

1991 ◽  
Vol 274 (3) ◽  
pp. 673-678 ◽  
Author(s):  
M Gianni ◽  
M Studer ◽  
G Carpani ◽  
M Terao ◽  
E Garattini
Keyword(s):  
Alkaline Phosphatase ◽  
Retinoic Acid ◽  
De Novo ◽  
F9 Cells ◽  
Alp Activity ◽  
Mrna Induction ◽  
All Trans Retinoic Acid ◽  
Teratocarcinoma Cells ◽  
F9 Teratocarcinoma ◽  
De Novo Protein Synthesis

All-trans retinoic acid (RA) induces alkaline phosphatase (ALP) activity by 3-8-fold in murine F9 teratocarcinoma cells, in parallel with their differentiation towards primitive endoderm. The elevation of ALP activity is associated with increases in the amounts of liver/bone/kidney-type ALP protein and the respective transcript. These effects of RA are due to activation of ALP gene transcription rather than to an increase in the half-life of the mRNA. Induction of ALP mRNA does not require de novo protein synthesis, since it is not blocked by treatment with cycloheximide. Dibutyryl cyclic AMP, which is known to induce further differentiation of F9 cells from the primitive to the parietal endoderm, blocks the induction of ALP mRNA by RA.

scholarly journals Tal2 expression is induced by all-trans retinoic acid in P19 cells prior to acquisition of neural fate

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Takanobu Kobayashi ◽  
Rie Komori ◽  
Kiyoshi Ishida ◽  
Katsuhito Kino ◽  
Sei-ichi Tanuma ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
P19 Cells ◽  
Neural Fate ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

9-cis and all-trans retinoic acid induce a similar phenotype in human teratocarcinoma cells

1993 ◽  
Vol 54 (3) ◽  
pp. 123-129 ◽  
Author(s):  
Jonathan M. Kurie ◽  
Jochen Buck ◽  
Thomas M. Eppinger ◽  
Denise Moy ◽  
Ethan Dmitrovsky
Keyword(s):  
Retinoic Acid ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Teratocarcinoma Cells ◽  
Similar Phenotype

scholarly journals Structure-activity relationships of retinoids as inhibitors of calmodulin-dependent human erythrocyte Ca2+-ATPase activity and calmodulin binding to membranes

1991 ◽  
Vol 277 (3) ◽  
pp. 603-606 ◽  
Author(s):  
F B Davis ◽  
T J Smith ◽  
P J Davis ◽  
S D Blas
Keyword(s):  
Enzyme Activity ◽  
Retinoic Acid ◽  
Atpase Activity ◽  
Human Erythrocyte ◽  
Enzyme Inhibitors ◽  
Ring Structure ◽  
Erythrocyte Membranes ◽  
Calmodulin Binding ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

All-trans retinoic acid displaces the binding of radiolabelled calmodulin to human erythrocyte membranes, and inhibits the activity of plasma membrane Ca(2+)-stimulated, Mg(2+)-dependent ATPase (Ca(2+)-ATPase; EC 3.6.1.3). This enzyme is dependent upon the action of calmodulin. In this study we explored the structural attributes of the retinoids which confer this ability to inhibit enzyme activity and calmodulin binding. With respect to the fatty acid side-chain, a clear requirement for inhibition is a trans-configuration of the polar end-group. The importance of the ring structure is indicated by the ineffectiveness of polyprenoic acid and a benzene ring retinoid analogue as inhibitors of enzyme activity and calmodulin binding. There was good correlation between the relative potencies of the analogues as enzyme inhibitors and as inhibitors of calmodulin binding. The ability of selected retinoid analogues, at physiological concentrations with respect to all-trans retinoic acid, to inhibit erythrocyte Ca(2+)-ATPase activity and membrane binding of calmodulin underscores the structurally specific effects of these compounds on the interaction of calmodulin with the membrane-bound enzyme.

scholarly journals All-trans retinoic acid mediates DUOX2 expression and function in respiratory tract epithelium

2010 ◽  
Vol 299 (2) ◽  
pp. L215-L221 ◽  
Author(s):  
Angela Lee Linderholm ◽  
June Onitsuka ◽  
Changhong Xu ◽  
Maggie Chiu ◽  
Wai-Ming Lee ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Respiratory Tract ◽  
Fold Increase ◽  
Respiratory Epithelial Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Mrna And Protein Expression ◽  
And Function ◽  
Respiratory Epithelial

DUOX1 and DUOX2 are members of the NADPH oxidase family that are specifically regulated to produce hydrogen peroxide in epithelia of the thyroid, gastrointestinal tract, and respiratory tract. The determinants of DUOX1 or DUOX2 expression in various tissues have not been established. Using respiratory tract epithelial cells as a model, we investigated changes in DUOX mRNA and protein expression during the first 10 days of differentiation. By comparing a respiratory tract cell line, HBE1, with primary tracheobronchial epithelial (TBE) cells, we determined that DUOX2 was significantly expressed only in cell conditions that included all- trans retinoic acid (ATRA). In HBE1 cells, DUOX2 mRNA increased 6-fold after ATRA treatment. Similarly, ATRA induced a 19-fold increase in DUOX2 mRNA expression in primary TBE cells with parallel increases in DUOX protein and DUOX-mediated H2O2 production as well. In addition, DUOX2 induction by rhinovirus required the presence of ATRA. ATRA had no effect on DUOX1 expression for all the conditions studied. Our data indicate that for respiratory epithelial cells, ATRA is important in the regulation of DUOX2 expression, function, and rhinovirus-mediated DUOX2 inducibility.

Maintenance of retinoic acid receptor alpha pools by granulocyte colony-stimulating factor and lithium chloride in all-trans retinoic acid–treated WEHI-3B leukemia cells: relevance to the synergistic induction of terminal differentiation

Blood ◽  
2000 ◽  
Vol 96 (6) ◽  
pp. 2262-2268 ◽  
Author(s):  
Rick A. Finch ◽  
Jianming Li ◽  
T-C. Chou ◽  
Alan C. Sartorelli
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Terminal Differentiation ◽  
Fold Increase ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
D Cells ◽  
Stimulating Factor

Abstract Previous studies have demonstrated that combinations of all-trans retinoic acid (ATRA) with either granulocyte-colony stimulating factor (G-CSF) or lithium chloride (LiCl) produced synergistic terminal differentiation of WEHI-3B myelomonocytic leukemia (D+) cells. It was found that steady-state retinoic acid receptor alpha (RARα) protein levels were markedly reduced in these cells after exposure to ATRA. Because the presence of receptors for a hormone ligand is required for its action, differentiation therapy with ATRA may be self-limiting. The combination of G-CSF with ATRA significantly attenuated the loss of RARα protein, and synergistic terminal differentiation occurred. LiCl was more effective than G-CSF in preserving RARα pools and synergized with ATRA more strongly than G-CSF. These findings suggested that the prevention of RARα protein loss by G-CSF or LiCl in ATRA-treated cells functioned to extend the differentiation response to the retinoid and was responsible, at least in part, for the observed synergism. D+ cells transfected with an expression plasmid containing RARα cDNA had a 6- to 8-fold increase in steady-state RARα mRNA compared with vector-transfected cells and showed a 2- to 3-fold increase in RARα protein. ATRA caused a reduction, but not a complete loss, of RARα protein in these transfectants, which were considerably more responsive than parental D+ cells to ATRA as a single agent, supporting the concept that the protection of RARα pools results in a heightened differentiation response to ATRA.

scholarly journals Retinoic acid and cyclic AMP synergistically induce the expression of liver/bone/kidney-type alkaline phosphatase gene in L929 fibroblastic cells

1993 ◽  
Vol 296 (1) ◽  
pp. 67-77 ◽  
Author(s):  
M Giannì ◽  
M Terao ◽  
S Sozzani ◽  
E Garattini
Keyword(s):  
Alkaline Phosphatase ◽  
Retinoic Acid ◽  
Cyclic Amp ◽  
Retinoic Acid Receptor ◽  
Pcr Amplification ◽  
Enzymic Activity ◽  
Dibutyryl Camp ◽  
All Trans Retinoic Acid ◽  
Steady State Levels ◽  
Fibroblastic Cells

In L929 mouse fibroblastic cells, liver/bone/kidney type alkaline phosphatase (L/B/K-ALP) enzymic activity is induced by all-trans-retinoic acid at concentrations between 10(-6) and 10(-5) M. At lower concentrations, retinoic acid is incapable of inducing this enzymic activity per se, but increases cyclic AMP (cAMP)-mediated induction. This effect is observed after incubation of the retinoid with dibutyryl cAMP, 8-bromo cAMP or forskolin. The synergism is dependent on the order of addition of retinoic acid and the activator of the cAMP pathway. Contemporaneous addition of the two agents, or addition of cAMP prior to retinoic acid (but not addition of retinoic acid before cAMP), is necessary to produce this synergistic interaction. The synergism results in increased steady-state levels of L/B/K-ALP mRNA and it is the consequence of increased transcriptional activity of the gene. The expression of the mouse L/B/K-ALP gene is regulated by the presence of two leader exons, 1A and 1B, resulting in the synthesis of two alternatively spliced mRNAs that are different only in part of their 5′ untranslated region [Studer, Terao, Giannì and Garattini (1991) Biochem. Biophys. Res. Commun. 179, 1352-1360]. PCR amplification and nuclear run-on experiments performed using probes specific for each leader exon demonstrate that treatment of these cells with retinoic acid, forskolin or dibutyryl cAMP, and with the combination of the retinoid and one of the cAMP-elevating agents, leads to the accumulation of nascent and mature L/B/K-ALP mRNA containing exon 1B. The synergistic induction of the transcription of the L/B/K-ALP gene is well correlated with quantitative and qualitative changes of retinoic-acid-receptor mRNAs mediated by cAMP.

Maintenance of retinoic acid receptor alpha pools by granulocyte colony-stimulating factor and lithium chloride in all-trans retinoic acid–treated WEHI-3B leukemia cells: relevance to the synergistic induction of terminal differentiation

Blood ◽  
2000 ◽  
Vol 96 (6) ◽  
pp. 2262-2268 ◽  
Author(s):  
Rick A. Finch ◽  
Jianming Li ◽  
T-C. Chou ◽  
Alan C. Sartorelli
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Terminal Differentiation ◽  
Fold Increase ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
D Cells ◽  
Stimulating Factor

Previous studies have demonstrated that combinations of all-trans retinoic acid (ATRA) with either granulocyte-colony stimulating factor (G-CSF) or lithium chloride (LiCl) produced synergistic terminal differentiation of WEHI-3B myelomonocytic leukemia (D+) cells. It was found that steady-state retinoic acid receptor alpha (RARα) protein levels were markedly reduced in these cells after exposure to ATRA. Because the presence of receptors for a hormone ligand is required for its action, differentiation therapy with ATRA may be self-limiting. The combination of G-CSF with ATRA significantly attenuated the loss of RARα protein, and synergistic terminal differentiation occurred. LiCl was more effective than G-CSF in preserving RARα pools and synergized with ATRA more strongly than G-CSF. These findings suggested that the prevention of RARα protein loss by G-CSF or LiCl in ATRA-treated cells functioned to extend the differentiation response to the retinoid and was responsible, at least in part, for the observed synergism. D+ cells transfected with an expression plasmid containing RARα cDNA had a 6- to 8-fold increase in steady-state RARα mRNA compared with vector-transfected cells and showed a 2- to 3-fold increase in RARα protein. ATRA caused a reduction, but not a complete loss, of RARα protein in these transfectants, which were considerably more responsive than parental D+ cells to ATRA as a single agent, supporting the concept that the protection of RARα pools results in a heightened differentiation response to ATRA.

9-cis and all-trans retinoic acid induce a similar phenotype in human teratocarcinoma cells

1993 ◽  
Vol 54 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Jonathan M. Kurie ◽  
Jochen Buck ◽  
Thomas M. Eppinger ◽  
Denise Moy ◽  
Ethan Dmitrovsky
Keyword(s):  
Retinoic Acid ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Teratocarcinoma Cells ◽  
Similar Phenotype
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